Your Brain on Botox

There is overwhelming evidence from animal studies, as well as foodborne and iatrogenic botulism case studies, that Botox can and does travel into the central nervous system (CNS).

This can happen when the toxin crosses the blood-brain barrier, or through a process called retrograde axonal transport, where botulinum toxin travels through nerve cells (neurons) from the site of injection into the CNS.

So...what the heck can Botox do in our brains?

Well, it turns out that Botox can block much more than acetylcholine once it enters the CNS.

As far back as 2004, Luvisetto et al, while experimenting on rats, reported, "Compared to control mice, BoNT-treated mice showed...a reduced capacity to discriminate a novel object within a familiar environment." (This was interpreted as cognitive impairments in the treated rats).

In 2012, Akaike et al reported,"Type A botulinum toxin blocks not only ACh (acetylcholine) release from motor nerve terminals but also central synaptic transmission, including glutamate, noradrenaline, dopamine, ATP, GABA and glycine. Neurotoxins (NTXs) are transported by both antero- and retrogradely along either motor or sensory axons for bidirectional delivery between peripheral tissues or the CNS."

For a quick reference, here are just a few of the things that those other neurotransmitters/neuromodulators do in our brain (information below obtained from www.ClevelandClinic.org)

Glutamate:

• helps us learn and make new memories

• regulates our sleep/wake cycle

• energy source for brain cells

• is necessary to make GABA

GABA:

• reduces stress

• relieves anxiety

• helps us sleep

Noradrenaline:

• increases alertness, arousal, and attention

Dopamine:

• regulates movement, memory, sleep/wake cycle, mood, learning, among others

Glycine:

• supports sleep quality

• supports cognitive function

In both foodborne and iatrogenic botulism cases, severe CNS disruption has been reported. If the toxin travels into the CNS via retrograde axonal transport, it wouldn't always enter the bloodstream, which means it's possible to have botulinum toxin travel to the CNS (brain) and disrupt function, without necessarily displaying typical peripheral nervous system (PNS) botulism symptoms (muscle weakness, difficulty swallowing, fatigue, dry mouth, etc.). (Although most people who experience botulism will have both PNS and CNS symptoms.)

In a 2024 case study report that looked at six people who had acquired foodborne botulism, researchers found that, "...all six family members reported subjective cognitive impairments more than 2.5 years post-infection. The cognitive reductions were not confined to a single cognitive domain but appeared to affect processing speed, attention span and shifts, memory, and executive functioning. Neuropsychological testing indicated mild-to-moderate cognitive impairments concerning attention and executive functioning. Furthermore, a declining processing speed indicated increasing effects of fatigue during testing sessions."

In Dr. Hristova's 2016 paper, which followed patients with iatrogenic botulism for more than four years, she wrote:

"Research has established that botulinum can block many mediators in CNS...Most of the patients presented here exhibit combined features of depletion of some mediators and increment of others" and,

"Patients often use the following expressions: 'I am in a fog… …I am in a bubble…I feel detached…My body is not listening to my brain…I am disconnected…Somebody else is operating my body'. The most common symptoms are impaired concentration, word finding difficulties, impairment of memory, significant head pressure, phono- and photophobia and inability to multitask. Processing speed is decreased. Events happening at a faster speed are not perceived well, such as: retrieving all information from a person speaking quickly or from a group of people speaking at the same time reading and looking at fast moving objects. Most of all, there is a mental fatigue which often leaves the patients debilitated and with the ability to only do a few tasks before exhaustion sets in."

A 2018 article looked at brain changes in iatrogenic botulism patients using fMRI. They found "Compared with the controls, the patients with botulism exhibited significantly reduced ReHo values (brain activity) in the left posterior lobe of the cerebellum extending to the right anterior lobe of the cerebellum, as well as in the right anterior lobe of the cerebellum extending to the parahippocampal gyrus and right posterior lobe of the cerebellum. The patients with botulism also showed weakened ALFF values (measuring signal intensity) in the right anterior lobe of the cerebellum extending to the left anterior lobe of the cerebellum and right posterior lobe of the cerebellum, as well as in the right anterior lobe of the cerebellum."

--the parahippocampal gyrus plays an important role in episodic memory and interpreting contextual and spacial information

--the cerebellum has many motor and cognitive functions, some of which include:

• Attention and executive control

• Language processing

• Spatial and temporal processing

• Working memory

• Emotional processing

Jean Carruthers, the "grandmother of Botox" (as I call her), seems to think that the potential Botox has to travel to our brains is a GOOD thing. She's marketing this "wonderful side effect" of Botox as a potential treatment for depression.

In this video, (beginning at minute 10:29), you can see her excitedly explaining how Botox can travel from the site of injection into the "anterior inferior temporal gyrus" and block critical neurotransmitter functioning there (she claims this was demonstrated on fMRI). The inferior temporal gyrus is involved in visual and semantic processing, as well as emotional regulation. Is attempting to "cure" depression (which is typically a multi-factorial, complex illness that should be treated in an individualized manner) by injecting a neurotoxin into our foreheads in the hopes that it will hop back along nerve cells and block essential cognitive functioning really a good idea? Me thinks not.

In the early months after I experienced toxin spread following 12 units of Xeomin (once!), I experienced bizarre cognitive symptoms that I had never had before in my life, including:

• short term memory loss - I had difficulty recalling past/upcoming events, past conversations, and would regularly forget appointments

• slow processing speed - when my husband would tell me something, I would take 10-15 seconds to process it and respond appropriately

• disorganization/confusion - I was putting refridgerated items into the pantry (regularly)

• brain fog that made me feel as if I was drugged and/or drunk (but without any "fun" feelings)

Botulism is not as simple of a disease as Google would like you to believe, and in 2025 the evidence is overwhelming: if Botox spreads into your brain, you could experience severe cognitive and psychiatric symptoms. This can happen with any amount of toxin, with any injector, at any time, even if you've never experienced a single side effect from Botox in 10+ years.

Allergan isn't even trying to deny that Botox can get into our brains anymore, they're simply spinning it to try to market it as a "treatment" for CNS disorders, like depression and seizures.

And that should scare every single one of us.

References:

Akaike N, Shin MC, Wakita M, Torii Y, Harakawa T, Ginnaga A, Kato K, Kaji R, Kozaki S. Transsynaptic inhibition of spinal transmission by A2 botulinum toxin. J Physiol. 2013 Feb 15;591(4):1031-43. doi: 10.1113/jphysiol.2012.242131. Epub 2012 Oct 29. PMID: 23109108; PMCID: PMC3591713.

Luvisetto S. Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy. Toxins (Basel). 2021 Oct 22;13(11):751. doi: 10.3390/toxins13110751. PMID: 34822535; PMCID: PMC8622321.

Restani L, Novelli E, Bottari D, Leone P, Barone I, Galli-Resta L, Strettoi E, Caleo M. Botulinum neurotoxin A impairs neurotransmission following retrograde transynaptic transport. Traffic. 2012 Aug;13(8):1083-9. doi: 10.1111/j.1600-0854.2012.01369.x. Epub 2012 May 9. PMID: 22519601.

Wang T, Martin S, Papadopulos A, Harper CB, Mavlyutov TA, Niranjan D, Glass NR, Cooper-White JJ, Sibarita JB, Choquet D, Davletov B, Meunier FA. Control of autophagosome axonal retrograde flux by presynaptic activity unveiled using botulinum neurotoxin type a. J Neurosci. 2015 Apr 15;35(15):6179-94. doi: 10.1523/JNEUROSCI.3757-14.2015. PMID: 25878289; PMCID: PMC4787026.